AimTo investigate the beneficial effects of nonpeptide angiotensin-(1-7)［Ang-(1-7)］ analogue AVE0991 on ventricular remodeling and cardiac dysfunction in rats induced by myocardial infarction (MI). Methods Forty male Sprague-Dawley rats were randomly divided into sham operation group, control group, AVE0991 group and AVE0991 + A-779 group. MI was induced by left coronary artery ligation. After 4 weeks of treatment, transthoracic echocardiography (TTE) was used to evaluate cardiac function. The left ventricle wet weight was recorded, normalized for body weight. Left ventricle serial sections were dyed with Masson or hematoxylin-eosin (HE) stain to quantify the infarct size and diameter measurement of cardiomyocytes. ResultsFour weeks after MI, rats with MI demonstrated significantly increase in the left ventricular end-diastolic (LVDd) and end-systolic dimension (LVDs) and decrease in interventricular septum end-systolic (IVSs) and end-diastolic thickness (IVSd), left ventricular fractional shorting (LVFS) and left ventricular ejection fraction (LVEF). AVE0991 treatment attenuated the decrease in LVFS (25.5 % ± 7.3 % vs 18.4 % ± 3.3 %, p<0.05) and LVEF (44.8% ± 7.6% vs 32.7% ± 6.5 %, p<0.05) compared to control group. AVE0991 also reduced MI-induced hypertrophy as quantified by myocyte diameter measurements (vs control group, 17.6± 2.4 μm vs 22.9± 3.9 μm, p< 0.05). In addition, left ventricular mass index (LVMI) (2.54 ± 0.25 vs 2.93 ± 0.34, p<0.01) and infarct size (42.6 % ± 3.6 % vs 50.9 % ± 4.4 %, p<0.01) were slightly reduced in AVE0991 group compared to control group. In addition, the specific antagonist for Ang-(1-7), ［D-Ala7］-Ang-(1-7) (A-779), showed a tendency to diminish the protective effects of AVE0991. ConclusionAVE0991 could attenuate ventricular remodeling and improve cardiac function induced by acute myocardial infarction in rats, its effects may play a role through the specific Mas receptor for Ang-(1-7).